The autonomic nervous system (ANS) regulates “involuntary” organs, while the contraction of voluntary (skeletal) muscles is controlled by somatic motor nerves. Examples of involuntary organs include respiratory and digestive organs, and also include blood vessels and the heart. Often, the ANS functions in an involuntary, reflexive manner to regulate glands, to regulate muscles in the skin, eye, stomach, intestines and bladder, and to regulate cardiac muscle and the muscle around blood vessels, for example.
The ANS includes the sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous system is affiliated with stress and the “fight or flight response” to emergencies. Among other effects, the “fight or flight response” increases blood pressure and heart rate to increase skeletal muscle blood flow, and decreases digestion to provide the energy for “fighting or fleeing.” The parasympathetic nervous system is affiliated with relaxation and the “rest and digest response” which, among other effects, decreases blood pressure and heart rate, and increases digestion to conserve energy. The ANS maintains normal internal function and works with the somatic nervous system. Afferent nerves convey impulses toward a nerve center, and efferent nerves convey impulses away from a nerve center.
The heart rate and force is increased when the sympathetic nervous system is stimulated, and is decreased when the sympathetic nervous system is inhibited (the parasympathetic nervous system is stimulated). Cardiac rate, contractility, and excitability are known to be modulated by centrally mediated reflex pathways. Baroreceptors and chemoreceptors in the heart, great vessels, and lungs, transmit cardiac activity through vagal and sympathetic afferent fibers to the central nervous system. Activation of sympathetic afferents triggers reflex sympathetic activation, parasympathetic inhibition, vasoconstriction, and tachycardia. In contrast, parasympathetic activation results in bradycardia, vasodilation, and inhibition of vasopressin release. Among many other factors, decreased parasympathetic or vagal tone or increased sympathetic tone is associated with various arrhythmias genesis, including ventricular tachycardia and atrial fibrillation.
Stimulating the sympathetic and parasympathetic nervous systems can have effects other than heart rate and blood pressure. For example, stimulating the sympathetic nervous system dilates the pupil, reduces saliva and mucus production, relaxes the bronchial muscle, reduces the successive waves of involuntary contraction (peristalsis) of the stomach and the motility of the stomach, increases the conversion of glycogen to glucose by the liver, decreases urine secretion by the kidneys, and relaxes the wall and closes the sphincter of the bladder. Stimulating the parasympathetic nervous system (inhibiting the sympathetic nervous system) constricts the pupil, increases saliva and mucus production, contracts the bronchial muscle, increases secretions and motility in the stomach and large intestine, and increases digestion in the small intention, increases urine secretion, and contracts the wall and relaxes the sphincter of the bladder. The functions associated with the sympathetic and parasympathetic nervous systems are many and can be complexly integrated with each other.
Neural stimulation can be used to stimulate nerve traffic or inhibit nerve traffic. An example of neural stimulation to stimulate nerve traffic is a lower frequency signal (e.g. within a range on the order of 20 Hz to 50 Hz). An example of neural stimulation to inhibit nerve traffic is a higher frequency signal (e.g. within a range on the order of 120 Hz to 150 Hz). Other methods for stimulating and inhibiting nerve traffic have been proposed. According to various embodiments of the present subject matter, sympathetic neural targets include, but are not limited to, a peroneal nerve, a sympathetic column in a spinal cord, and cardiac post-ganglionic sympathetic neurons. According to various embodiments of the present subject matter, parasympathetic neural targets include, but are not limited to, a vagus nerve, a baroreceptor, and a cardiac fat pad. Neural stimulation can be selectively delivered to afferent neural pathways, selectively delivered to efferent neural pathways, or delivered to both afferent and efferent neural pathways. For example, some embodiments selectively stimulate or inhibit only parasympathetic afferents or only parasympathetic efferents, and some embodiments selectively stimulate or inhibit sympathetic afferents or efferents.
The present subject matter can be used to prophylactically or therapeutically treat various diseases by modulating autonomic tone. Examples of such diseases or conditions include hypertension, cardiac remodeling, and heart failure.
Hypertension is a cause of heart disease and other related cardiac co-morbidities. Hypertension occurs when blood vessels constrict. As a result, the heart works harder to maintain flow at a higher blood pressure, which can contribute to heart failure. Hypertension generally relates to high blood pressure, such as a transitory or sustained elevation of systemic arterial blood pressure to a level that is likely to induce cardiovascular damage or other adverse consequences. Hypertension has been defined as a systolic blood pressure above 140 mm Hg or a diastolic blood pressure above 90 mm Hg. Consequences of uncontrolled hypertension include, but are not limited to, retinal vascular disease and stroke, left ventricular hypertrophy and failure, myocardial infarction, dissecting aneurysm, and renovascular disease. A large segment of the general population, as well as a large segment of patients implanted with pacemakers or defibrillators suffer from hypertension. The long term mortality as well as the quality of life can be improved for this population if blood pressure and hypertension can be reduced. Many patients who suffer from hypertension do not respond to treatment, such as treatments related to lifestyle changes and hypertension drugs.
Following myocardial infarction (MI) or other cause of decreased cardiac output, a complex remodeling process of the ventricles occurs that involves structural, biochemical, neurohormonal, and electrophysiologic factors. Ventricular remodeling is triggered by a physiological compensatory mechanism that acts to increase cardiac output due to so-called backward failure which increases the diastolic filling pressure of the ventricles and thereby increases the so-called preload (i.e., the degree to which the ventricles are stretched by the volume of blood in the ventricles at the end of diastole). An increase in preload causes an increase in stroke volume during systole, a phenomena known as the FrankStarling principle. When the ventricles are stretched due to the increased preload over a period of time, however, the ventricles become dilated. The enlargement of the ventricular volume causes increased ventricular wall stress at a given systolic pressure. Along with the increased pressure-volume work done by the ventricle, this acts as a stimulus for hypertrophy of the ventricular myocardium. The disadvantage of dilatation is the extra workload imposed on normal, residual myocardium and the increase in wall tension (Laplace's Law) which represent the stimulus for hypertrophy. If hypertrophy is not adequate to match increased tension, a vicious cycle ensues which causes further and progressive dilatation. As the heart begins to dilate, afferent baroreceptor and cardiopulmonary receptor signals are sent to the vasomotor central nervous system control center, which responds with hormonal secretion and sympathetic discharge. It is the combination of hemodynamic, sympathetic nervous system and hormonal alterations (such as presence or absence of angiotensin converting enzyme (ACE) activity) that ultimately account for the deleterious alterations in cell structure involved in ventricular remodeling. The sustained stresses causing hypertrophy induce apoptosis (i.e., programmed cell death) of cardiac muscle cells and eventual wall thinning which causes further deterioration in cardiac function. Thus, although ventricular dilation and hypertrophy may at first be compensatory and increase cardiac output, the processes ultimately result in both systolic and diastolic dysfunction (decompensation). It has been shown that the extent of ventricular remodeling is positively correlated with increased mortality in post-MI and heart failure patients.
Heart failure refers to a clinical syndrome in which cardiac function causes a below normal cardiac output that can fall below a level adequate to meet the metabolic demand of peripheral tissues. Heart failure may present itself as congestive heart failure (CHF) due to the accompanying venous and pulmonary congestion. Heart failure can be due to a variety of etiologies such as ischemic heart disease. Heart failure patients have reduced autonomic balance, which is associated with LV dysfunction and increased mortality. Modulation of the sympathetic and parasympathetic nervous systems has potential clinical benefit in preventing remodeling and death in heart failure and post-MI patients. Direct electrical stimulation can activate the baroreflex, inducing a reduction of sympathetic nerve activity and reducing blood pressure by decreasing vascular resistance. Sympathetic inhibition and parasympathetic activation have been associated with reduced arrhythmia vulnerability following a myocardial infarction, presumably by increasing collateral perfusion of the acutely ischemic myocardium and decreasing myocardial damage.
The prior art teaches many way of measuring heart rate. A stethoscope is traditionally used to amplify these sounds and present them to a caregiver. The acoustic principle may also be used in other ways, both manual and automated, at various parts of the body. Another way is the pulse oximeter approach. In pulse oximeters, a light of a known frequency through an area of the body, such as the fingertip or earlobe, and detect the same light once it has either passed through the body or been reflected back to a photo sensor. With each heart beat, oxygen-rich blood is momentarily pushed through the capillaries in that region. This momentary increase in the oxygen content of the blood upon each heart beat changes the optical properties of the blood. As the light passes through the fingertip or earlobe, specific frequencies are absorbed to varying degrees, depending on the amount of oxygen in the blood, and are therefore not present in the returning light. The change in detected frequencies occurring once per heart beat allows for detection of individual heart beats, and thus a heart rate measurement. The degree of spectral change is used to determine the oxygen content in the blood. Another measurement method makes use of the varying outward pressure applied against the skin by major arteries. With each heart beat, a surge of blood passes through the arteries. In an artery of sufficient size, and located near to the surface of the body, this momentary pressure can be detected by holding a pressure sensor, such as a piezo-electric (P-E) element, in place over the artery location. The P-E element is physically stretched by the momentary outward pressure of the artery during a heart-beat. As it is stretched, the altered shape of the P-E element changes its electrical characteristics—e.g., a change in its resistance to a current passing through it. Changes in the resistance of the P-E are then detected by appropriate circuitry, and used to identify heart beats and thus heart rate. Suitable surface arteries and sensing devices are well known in the art and include sensing at the wearer's wrist, the temple, the inner ear, or the bridge of the nose.
Heart rate monitoring using the chest strap method has become increasingly popular for sports and fitness training as well as for some other activities such as relaxation training, stress relief and meditation in which heart rate as a bio-feedback item has been found useful. During this time, the chest strap has remained in much the same form, as a practical means of obtaining a continuous, accurate heart rate reading for these largely non-medical purposes. However, for many users, the chest strap may chafe causing discomfort. Many users find them awkward to put on, uncomfortable to wear, and bothersome to keep handy. In addition, they can be restrictive of good chest expansion and thus restrict full breathing during exercise. For wearers with slender ribs and torsos, the chest strap can slip down out of the proper position and cease to function properly. Stretched across the chest, they are perceived by some as unmanly, or unwomanly, or as interfering with tan lines or undergarments.
There are various physiological factors affecting the autonomic regulation of heart rate: respiration, thermoregulation, hormonal regulation, blood pressure, cardiac output, etc. One of the most important factors is blood pressure. There are special cells in the heart and large blood vessels that sense blood pressure level and send afferent stimulation to the central structures of the ANS that control HR and blood vessel tonus forming a continuous feedback to maintain an optimal level of the blood pressure.
This mechanism is also called baroreflex. It increases HR when blood pressure drops and vice versa and thus maintains a short-term stable blood supply to the vital organs.
One of the best ways to assess the autonomic function is to analyze minute changes in heart rate, which are caused by many factors including regulatory influence of the autonomic nervous system.
A special method of analysis can be applied to recorded heart rate readings. It is called Heart Rate Variability (HRV) analysis. The HRV analysis is a powerful, very accurate, reliable, reproducible, yet simple to do.
It is found that lowered HRV is associated with aging, decreased autonomic activity, hormonal tonus, specific types of autonomic neuropathies (e.g. diabetic neuropathy) and increased risk of sudden cardiac death after acute heart attack.
Other research indicated that depression, panic disorders and anxiety have negative impact on autonomic function, typically causing depletion of the parasympathetic tonus. On the other hand an increased sympathetic tonus is associated with lowered threshold of ventricular fibrillation. These two factors could explain why such autonomic imbalance caused by significant mental and emotional stress increases risk of heart attack followed by sudden cardiac death.
Aside from that, there are multiple studies indicating that HRV is quite useful as a way to quantitatively measure physiological changes caused by various interventions both pharmacological and non-pharmacological during treatment of many pathological conditions having significant manifestation of lowered HRV.
However it is important to realize that clinical implication of HRV analysis has been clearly recognized as a predictor of risk of arrhythmic events or sudden cardiac death after acute heart attack, and as clinical marker of diabetic neuropathy evolution.
Nevertheless, as the number of clinical studies involving HRV in various clinical aspects and conditions grows, HRV remains one of the most promising methods of investigating general health in the future.
There is an ongoing need for an improved system and method for heart rate, heart rate variability, wellness and fitness monitoring that is user friendly and less invasive.